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There have been reported cases of onset or exacerbation of inflammatory arthritis following traumatic events.1–11 In this type of situation there is always uncertainty as to whether the trauma was truly the inciting event or whether the timing was merely coincidental. In the event of a workplace injury and subsequent development of inflammatory arthritis, physicians might be asked to formally address causal relationships in reference to claims to the Workers’ Compensation Board (WCB) or other compensatory financial institutions. In this report we relate a further case study of exacerbation of psoriatic arthritis following a traumatic injury and review the literature addressing this potential association.
A 39-year-old man with a 14-year history of seronegative inflammatory polyarthritis was diagnosed with psoriatic arthritis. His test results were negative for the human leukocyte antigen B27 (HLA-B27). He had long-standing dactylitic involvement of the third and fourth left digits, and occasionally observed swelling of the fourth right metacarpophalangeal joint. He had been treated over time with nonsteroidal anti-inflammatory drugs, sulfasalazine, and methotrexate. He did have occasional self-determined interruptions in his pharmacotherapy and periodically had transient inflammatory flares in other regions, including dactylitic involvement in his toes, ankle swelling, and knee effusions. However, his disease had been quite stable with the use of methotrexate for some time. Between October and November of 2009 the patient discontinued taking all medications. His rheumatology follow-up visit in March 2010 documented no new joint swelling on physical examination and specifically no joint or digit swelling on the right hand.
In late July 2010 he suffered a crush injury to his right hand during the course of his work as a house painter. His hand, particularly the third digit and to a lesser extent the fourth digit, became swollen, erythematous, and painful (Figure 1). Radiographs taken immediately after the injury did not demonstrate any fracture or bony abnormality. Magnetic resonance imaging of the third digit, which was taken 2 months after the injury, demonstrated changes consistent with dactylitis, bone marrow edema, and third-digit flexor tenosynovitis (Figure 2). The digital swelling and discomfort persisted with decreased ability to flex the digits. In October 2010 the patient returned to the rheumatology clinic for follow-up. Radiographs taken during this visit demonstrated soft tissue swelling of the third digit and erosive changes of the fourth proximal interphalangeal joint (Figure 3). His C-reactive protein level was elevated at 10.2 mg/L. Although initially the patient had been reluctant to consider further pharmacotherapy, at this point he consented to reinitiation of methotrexate and nonsteroidal anti-inflammatory drug therapy. In January 2011 repeat magnetic resonance imaging revealed persistent bone marrow edema, soft tissue edema, synovitis, and early erosions in the third proximal phalanx at the proximal interphalangeal joint not yet visible on radiograph (Figure 4).Swollen and erythematous right third digit, with a lesser degree of involvement of the right fourth digitMagnetic resonance imaging of patient’s right hand (obtained with a limited field of view, excluding the proximal interphalangeal and distal interphalangeal joints): A) Coronal sequence. Edematous changes in the soft tissues (small white arrow) ...Radiograph of patient’s right hand in October 2010: Generalized soft tissue swelling is seen at the third phalanx with no third-digit erosions visible at this time. Erosions (white arrows) are seen at the fourth proximal interphalangeal joint. ...Magnetic resonance imaging of patient’s right fingers in January 2011: A) Coronal gadolinium-enhanced image. Bone marrow edema (thick white arrows), synovial enhancement (black arrows), and soft tissue edema (thin white arrow) are found in the ...
The patient filed a workers’ compensation claim, which was subsequently denied. He is appealing this decision.
In the case of our patient, the inflammatory arthritis and dactylitis affecting the right hand developed in temporal proximity to a significant injury. There have been earlier case reports in the English-language literature of posttraumatic development or exacerbation of both seronegative and seropositive inflammatory arthropathies, which are summarized in Table 1.1–11 These reports exhibit varying degrees of temporal or physical proximity to the recalled injury. There have also been 2 case studies of patients with psoriatic skin disease who developed terminal acroosteolysis after a local traumatic event affecting the nails but without apparent articular involvement.12,13 Additionally, there have been several instances of posttraumatic initiation of inflammatory arthropathies reported in the non–English-language literature.3 These various individual histories are intriguing and assist in generating hypotheses; however, they are insufficient in themselves to unequivocally assign causality.
The cases described in Table 11–11 include seropositive rheumatoid arthritis, arthropathies associated with HLA-B27 positivity, reactive arthritis, and psoriasis-associated arthritis. Of the 22 cases detailed, 10 were associated with psoriatic or psoriaticlike skin lesions.
The concept of trauma as an inciting event in psoriatic arthritis seems to have originally arisen from the observation in the dermatology population of a Köbner phenomenon, whereby development of psoriatic skin disease has been observed at the sites of significant injury to the dermis and epidermis. It has been proposed that psoriatic arthritis after injury might reflect a “deep-Köbner” effect.12
To further evaluate the premise that trauma might be an inciting event in psoriatic arthritis, Scarpa et al undertook a retrospective chart review of the medical records of 138 patients with psoriatic arthritis and 138 patients with rheumatoid arthritis. A preceding acute event was documented in 9% of patients with psoriatic arthritis in the 10 days before onset of joint symptoms, compared with 1% of patients with rheumatoid arthritis. A preceding event was not found to be more common in patients with psoriatic arthritis who had positive HLAB27 status.14
Two recent retrospective case-control studies have been conducted to evaluate frequency of preceding trauma in patients with psoriatic arthritis. Thumboo and colleagues employed the Rochester Epidemiology Project database, securing 60 psoriatic arthritis cases and 120 control patients with psoriasis. Trauma was defined as documented motor vehicle accident, fracture, sprain or contusion, surgical procedure, or burn. The time frame extended to 2 years before onset of joint symptoms. There were no significant differences observed in odds ratios for either fractures or all forms of trauma between the psoriatic arthritis cases and the control group.15 The second case-control study was reported by Pattison et al and examined a UK population of 98 psoriatic arthritis cases and 163 control patients with psoriasis. Patients who developed psoriatic arthritis onset within 5 years of the selected study date were included. Physical trauma was defined as documented road traffic accidents, fractures, or other injuries requiring treatment by a general practitioner or at an accident and emergency department in the previous 10 years before the study date. The strongest association was with “trauma leading to medical care,” which applied to 14.9% of cases and 7.9% of controls for an odds ratio of 2.53 (95% CI 1.1 to 6.0).16
The multifaceted pathogenesis of psoriatic arthritis is an area of ongoing study. Evidence of genetic contribution predisposing to development of arthritis has been found in specific HLA allele associations and in identification of susceptibility genes.17 Support for a possible dysregulation of the innate immune response, particularly to bacterial antigenic stimulation, has also been reported.17 In terms of tissue-specific factors, recent persuasive work by McGonagle et al suggests the enthesis might be a key site for initiation of psoriatic arthritis, with enthesitis or osteitis preceding development of adjacent synovitis and joint damage.18,19 Enthesitis might be provoked by repeated microtrauma from shear and compressive stressing or by a more substantial single injury.
Although there is evidence for scientific rationale behind the proposed association between trauma and onset or exacerbation of psoriatic arthritis, and there have been case reports suggesting a causal link, case-control studies have not been in agreement on this question. This ambiguity in the literature makes it more challenging for the physician in a WCB claim situation to provide a just evaluation of a given clinical circumstance. In such workplace-related injuries, the “criteria of imputability” referred to by Olivieri might be of use.20 These criteria include the following: single and significant trauma; absence of joint lesions before trauma; localization of arthritis in the area of trauma; and absence of delay or short delay between trauma and onset of arthritis. Although it is likely that situations will arise in which such criteria will not be completely applicable, these criteria or similarly structured guidelines would be valuable to assist physicians in most posttraumatic psoriatic arthritis assessments.
This article has been peer reviewed.
Cet article a fait l’objet d’une révision par des pairs.